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  • Title: MAP kinase additively activates the mouse Per1 gene promoter with CaM kinase II.
    Author: Nomura K, Takeuchi Y, Fukunaga K.
    Journal: Brain Res; 2006 Nov 06; 1118(1):25-33. PubMed ID: 17020748.
    Abstract:
    In a previous study, we showed that the Ca2+/calmodulin-dependent protein kinase IIdelta (CaMKIIdelta) activates the mouse Per1 (mPer1) promoter through a 5'-GAGGGG-3' motif near exon1B. Here we use luciferase reporter gene assays to document additive activation of the mPer1 promoter by CaMKIIdelta and mitogen-activated protein kinase (MAPK) pathways. Transfection of constitutively active MEKK markedly increased mPer1 promoter activity in NB2A cells. Experiments using MAPK inhibitors and dominant-negative c-Jun NH2-terminal kinase 1 (JNK1) showed that extracellular signal-regulated kinase (ERK) accounts for MEKK-induced mPer1 gene activation. We next defined the ERK-responsive region in the mPer1 promoter. A region from -1735 to -1721 was required for ERK-induced promoter activation. We also identified a CaMKII-responsive element near exon 1B. Although mutation of the CaMKII-responsive element has no effect on the ERK responsiveness, elimination of a GC-rich sequence downstream of the CaMKII-responsive region totally abolished ERK responsiveness. Finally, ERK-induced promoter activation was additively potentiated by co-transfection with active CaMKIIdelta. These results suggest that additive activation by ERK and CaMKII, most likely as a result of photic stimulation in the suprachiasmatic nucleus, plays a critical role in activating the mPer1 gene promoter.
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